Recent Updates on Controversies in Decompressive Craniectomy and Cranioplasty: Physiological Effect, Indication, Complication, and Management

Abstract

Decompressive craniectomy (DCE) and cranioplasty (CP) are surgical procedures used to manage elevated intracranial pressure (ICP) in various clinical scenarios, including ischemic stroke, hemorrhagic stroke, and traumatic brain injury. The physiological changes following DCE, such as cerebral blood flow, perfusion, brain tissue oxygenation, and autoregulation, are essential for understanding the benefits and limitations of these procedures. A comprehensive literature search was conducted to systematically review the recent updates in DCE and CP, focusing on the fundamentals of DCE for ICP reduction, indications for DCE, optimal sizes and timing for DCE and CP, the syndrome of trephined, and the debate on suboccipital CP. The review highlights the need for further research on hemodynamic and metabolic indicators following DCE, particularly in relation to the pressure reactivity index. It provides recommendations for early CP within three months of controlling increased ICP to facilitate neurological recovery. Additionally, the review emphasizes the importance of considering suboccipital CP in patients with persistent headaches, cerebrospinal fluid leakage, or cerebellar sag after suboccipital craniectomy. A better understanding of the physiological effects, indications, complications, and management strategies for DCE and CP to control elevated ICP will help optimize patient outcomes and improve the overall effectiveness of these procedures.

Keywords: Craniocerebral trauma; Craniotomy; Decompressive craniectomy; Intracranial pressure.

FIGURE 1. The Monro-Kellie model illustrating the components of the intracranial compartment. This model demonstrates the delicate balance between brain tissue, CSF, and blood within the rigid skull. ‘Brain tissue’ encompasses neurons, glia, extracellular fluid, and cerebral microvasculature. ‘Venous’ and ‘arterial blood’ represent the intracranial blood volume in macrovasculature and cerebral venous sinuses. ‘CSF’ includes ventricular and cisternal CSF.

CSF: cerebrospinal fluid.

FIGURE 2. The Monro-Kellie Doctrine illustrating intracranial compensation mechanisms in response to an expanding mass. This doctrine demonstrates the complex interplay between brain tissue, CSF, and blood within the confined space of the skull. According to the Monro-Kellie Doctrine, when an expanding mass is introduced, compensatory mechanisms involving the reduction of one or both other components are employed to maintain constant intracranial pressure. These compensatory changes can reach a limit, after which further increases in mass may lead to rapid elevation of intracranial pressure and potential brain herniation.

ICP: intracranial pressure, CSF: cerebrospinal fluid.

FIGURE 3. Pressure-volume curve for ICP. This curve demonstrates the relationship between intracranial volume and ICP, with four distinct ‘zones’: (1) baseline intracranial volume with good compensatory reserve and high compliance (blue); (2) gradual depletion of compensatory reserve as intracranial volume increases (yellow); (3) poor compensatory reserve and increased risk of cerebral ischemia and herniation (red); and (4) critically high ICP causing collapse of cerebral microvasculature and disturbed cerebrovascular reactivity (grey). The curve highlights the importance of monitoring and managing ICP in clinical practice, as changes in intracranial volume can have significant implications for patient outcomes.

ICP: intracranial pressure.

FIGURE 4. Pressure-volume curve for ICP before and after decompressive craniectomy. The curve illustrates the relationship between intracranial volume and ICP, emphasizing the impact of DCE on the pressure-volume compensatory reserve (RAP). The red line represents the pressure-volume curve before decompressive craniectomy, while the red dot-line indicates the pressure-volume curve after decompressive craniectomy. Following decompressive craniectomy, there is an increase in the pressure-volume compensatory reserve, as demonstrated by the shift in the curve. This figure highlights the effectiveness of decompressive craniectomy in alleviating elevated ICP and improving intracranial compliance.

DCE: decompressive craniectomy, ICP: intracranial pressure, RAP: pressure-volume compensatory reserve.

FIGURE 5. ICP values at the each surgical steps The box plot illustrates the median ICP values (solid line within each box) and the interquartile range (p25 to p75) represented by the boxes. This figure highlights the variations in ICP throughout the surgical process, emphasizing the importance of each surgical procedures to decrease ICP during neurosurgical procedures to optimize patient outcomes.

ICP: intracranial pressure.

FIGURE 6. Treatment algorithm for cerebellar infarction.

EVD: extraventricular drainage, TLD: treat-limiting decision.

FIGURE 7. Illustration demonstrating the four theoretical mechanisms contributing to the syndrome of the trephined. (A) Atmospheric pressure: the absence of the skull bone exposes the brain to external atmospheric pressure, potentially causing deformation and functional disturbances. (B) Craniocaudal CSF flow: alterations in the CSF flow dynamics due to the skull defect may result in abnormal pressure gradients and impaired CSF circulation. (C) Decreased cerebral blood flow: the skull defect may lead to reduced cerebral perfusion, negatively impacting neuronal function. (D) Decreased cerebral metabolism: compromised energy metabolism and oxygen utilization in the affected brain tissue may contribute to the development of neurological symptoms. This figure highlights the complex interplay of factors involved in the pathophysiology of the syndrome of the trephined.

CSF: cerebrospinal fluid, PCr/Pi: phosphocreatine to inorganic phosphate ratio.